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Tardive Dyskinesia Treatment Options - Guidelines for Treating Tardive...
Tardive Dyskinesia Treatment Options - Guidelines for Treating Tardive...
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 Neurogenetics: Familial Paroxysmal Dyskinesia
Neurogenetics: Familial Paroxysmal Dyskinesia
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Dyskinesia
Classification and external resources
ICD-10 G24.9
ICD-9 333.8
DiseasesDB 17912
MeSH D020820

Dyskinesia is a movement disorder which consists of effects including diminished voluntary movements[1] and the presence of involuntary movements, similar to tics or chorea. Dyskinesia is a symptom of several medical disorders and is distinguished by the underlying cause. When a dyskinesia presents after treatment with an antipsychotic drug such as haloperidol (Haldol), it is known as tardive dyskinesia, and is commonly seen in the face and mouth in the form of 'tongue rolling'. Dyskinesia observed in a patient with Parkinson's disease (PD) is labeled as Levodopa-induced dyskinesia (LID), and is more commonly a jerky, dance-like movement of the arms and/or head, which usually presents after several years of treatment with L-DOPA (Levodopa). Two other types, primary ciliary dyskinesia, and biliary dyskinesia, are caused by specific kinds of ineffective movement of the body.

[edit] Parkinson's Disease

In the context of Parkinson's disease (PD), dyskinesia is often the result of chronic L-DOPA (Levodopa) therapy. These motor fluctuations occur in more than half of PD patients after 5–10 years of L-DOPA treatment, with the percentage of affected patients increasing over time.[2] Dyskinesia most commonly occurs at the time of peak L-DOPA plasma concentrations and is thus referred to as peak-dose dyskinesia (PDD). As patients advance, they may evidence diphasic dyskinesia (DD), which occur when the drug concentration rises or falls. Attempts to moderate dyskinesia by the use of other treatments such as bromocriptine (Parlodel) appears to be ineffective.[3] In order to avoid dyskinesia, patients with the young-onset form of the disease or young-onset Parkinson's disease (YOPD) are often hesitant to commence L-DOPA therapy until absolutely necessary for fear of suffering severe dyskinesia later on.

Patients with prominent dyskinesia resulting from high doses of antiparkinsonian medications may benefit from deep brain stimulation (DBS), which benefits the patient in two ways: 1) DBS allows a reduction in L-DOPA dosage of 50-60% (thus tackling the underlying cause); 2) DBS treatment itself (in the subthalamic nucleus or globus pallidus) can reduce dyskinesia.[4]

The use of methylenedioxymethamphetamine ("Ecstasy", "E", "X", "XTC", etc) has been shown to enhance the effects of L-DOPA while reducing the associated dyskinesia in primates with advanced PD.[5] Its serotonergic actions may be responsible for this effect.

[edit] See also

[edit] References

  1. ^ dyskinesia at Dorland's Medical Dictionary
  2. ^ Obeso JA, et al. The evolution and origin of motor complications in Parkinson's disease. Neurology. 2000;55 (suppl 4):S13-S20.
  3. ^ van Hilten J, Ramaker C, Stowe R, Ives Nj., 2007. Bromocriptine/levodopa combined versus levodopa alone for early Parkinson's disease. Cochrane Database Syst Rev. 2007 Oct 17;(4):CD003634.
  4. ^ Hiroki Toda, M.D., Ph.D.; Clement Hamani, M.D., Ph.D.; Andres Lozano, M.D., Ph.D., F.R.C.S.(C) 2004. Deep Brain Stimulation in the Treatment of Dyskinesia and Dystonia. Neurosurg Focus 17(1):9-13, 2004.
  5. ^ Iravani, M., Jackson, M., Kuoppamäki, M., Smith, L. & Jenner, P. (2003). 3,4-Methylenedioxymethamphetamine (Ecstasy) Inhibits Dyskinesia Expression and Normalizes Motor Activity in 1-Methyl-4-Phenyl-1,2,3,6-Tetrahydropyridine-Treated Primates, Journal of Neuroscience, 23, 9107–9115



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